Ludger Seipel

Prevalence of late potentials in patients with and without ventricular tachycardia: Correlation with angiographic findings

Late potentials occurring at the end of or after the QRS complex were searched for from the body surface using high gain amplification and signal averaging techniques with filter settings between 100 and 300 hertz. The number of repetitions of the averaging process ranged between 150 and 300. Two hundred thirty-six patients were studied. In 27 control subjects, no late potentials were recorded. Among 146 patients without ventricular tachycardia or fibrillation, late potentials were present in 49 (34 percent). The mean duration of late potentials was 31 +/- 15.3 ms (median 25). Of 63 patients with documented ventricular tachycardia or fibrillation, 45 (71 percent) had late potentials (mean duration 51 +/- 31.5 ms; median 50) (probability [p] greater than 0.001). There was a close correlation between the detection of late potentials and left ventricular function. Late potentials occurred more frequently in patients with than in those without ventricular akinesia or aneurysm and in patients with than in those without ventricular tachycardia or fibrillation. In conclusion, late potentials are a frequent finding in patients with regional contraction abnormalities, both in patients with and in those without documented ventricular tachycardia. The greater prevalence and longer duration of these signals in patients with ventricular tachycardia or fibrillation might be responsible for the greater susceptibility to ventricular tachycardia. Long-term follow-up studies will be necessary to assess the possible prognostic significance of late potentials in patients without previously documented ventricular tachycardia or fibrillation.

Clinical Experience with the New Detection Algorithms for Atrial Fibrillation of a Defibrillator with Dual Chamber Sensing and Pacing

ICD with DDD Pacemaker. Introduction: A major drawback of therapy with an implantable defibrillator is the nonspecificity of detection. Theoretically, adding atrial sensing information to a decision algorithm could improve specificity of detection.

Suppression of sustained ventricular tachyarrhythmias: a comparison of d,l-sotalol with no antiarrhythmic drug treatment

OBJECTIVESnThis study evaluates the clinical efficacy of d,l-sotalol in patients with sustained ventricular tachyarrhythmias.nnnBACKGROUNDnD,l-sotalol is an important antiarrhythmic agent to prevent recurrences of sustained ventricular tachyarrhythmias (VT/VF). However, evidence is lacking that an antiarrhythmic agent like d,l-sotalol can reduce the incidence of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.nnnMETHODSnA prospective study was performed in 146 consecutive patients with inducible sustained ventricular tachycardia or ventricular fibrillation. In 53 patients, oral d,l-sotalol prevented induction of VT/VF during electrophysiological testing and patients were discharged on oral d,l-sotalol (sotalol group). In 93 patients, VT/VF remained inducible and a defibrillator (ICD) was implanted. After implantation of the device patients were randomly assigned to oral treatment with d,l-sotalol (ICD/sotalol group, n=46) or no antiarrhythmic medication (n=47, ICD-only group).nnnRESULTSnDuring follow-up, 25 patients (53.2%) in the ICD-only group had a VT/VF recurrence in comparison to 15 patients (28.3%) in the sotalol group and 15 patients (32.6%) in the ICD/sotalol group (p=0.0013). Therapy with d,l-sotalol, amiodarone or metoprolol was instituted in 12 patients (25.5%) of the ICD-only group due to frequent VT/VF recurrences or symptomatic supraventricular tachyarrhythmias. In nine patients, 17% of the sotalol group, an ICD was implanted after VT/VF recurrence, three patients (5.7%) received amiodarone. Total mortality was not different between the three groups.nnnCONCLUSIONSnD,l-sotalol significantly reduces the incidence of recurrences of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.

Effect of propafenone in the wolff-parkinson-white syndrome: Electrophysiologic findings and long-term follow-up

The electrophysiologic and long-term efficacy of propafenone, a relatively new antiarrhythmic agent, was assessed in 47 patients with accessory pathways. In 23 patients (group I), the electrophysiologic effects were assessed initially. In 19 patients in this group and in 24 additional patients (group II), long-term therapy with oral propafenone was initiated. The mean age of the patients was 38 years in group I and 41 years in group II. The duration of a history of tachycardia in both groups was 12 years (mean); 14 patients previously had had attacks of syncope. During the electrophysiologic study in group I, propafenone did not change the spontaneous sinus rate. Corrected sinus node recovery time as well as the AH interval, HV time, QRS duration and effective refractory periods of the atria and ventricles was significantly prolonged. The effective refractory period of the accessory pathway increased from 238 to 322 ms (p less than 0.02). The 1:1 conduction capacity of the accessory pathway decreased from 231 to 176 beats/min (mean; p less than 0.01). Complete block in the anterograde direction occurred in 6 patients. The shortest RR interval during atrial fibrillation increased from 232 to 303 ms (p less than 0.05). The retrograde refractory period of the accessory pathway was prolonged from 245 to 295 ms (p less than 0.01). Complete or 2:1 retrograde block during basic drive occurred in 3 patients and 1 patient, respectively. In 6 of 15 patients, propafenone made sustained supraventricular tachycardia (SVT) either no longer inducible or nonsustained. The cycle length of induced SVT increased from 324 to 395 ms (p less than 0.01). During long-term administration (follow-up duration 2 to 3 years), 17 of 43 patients did not report any episode of symptomatic tachycardia. In another 18 patients, tachycardia was rare, slower and self-terminating. In only 3 patients, the frequency and severity of attacks had not changed. One patient with dilated cardiomyopathy died suddenly. Side effects necessitating discontinuation of medication were observed in only 2 patients. The remaining side effects, if present, were tolerated, and dosage dependent. In conclusion, propafenone is an effective and well-tolerated antiarrhythmic agent in the long-term management of patients with the Wolff-Parkinson-White syndrome.

Thrombolytic therapy in acute myocardial infarction : Comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the Kallikrein system and plasmin

BACKGROUNDnThrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI.nnnMETHODS AND RESULTSnSixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P<0.05) and kallikrein (up to 45+/-4 versus 30+/-1 U/L at 3 hours, P<0.01) activation occurs in patients with AMI. D-Dimers are increased (P<0.01), and plasmin is stimulated (P<0.01). Streptokinase and alteplase increase TAT to 50+/-17 and 51+/-18 microg/L at 3 hours and to 50+/-17 and 33+/-14 microg/L at 6 hours, respectively (P<0.01). Kallikrein activity is elevated (P<0. 01) to 76+/-5 and 71+/-7 U/L at 3 hours and 64+/-6 and 47+/-5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (P<0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (P<0.01).nnnCONCLUSIONSnThe data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.

Effects of antiarrhythmic surgery on late ventricular potentials recorded by precordial signal averaging in patients with ventricular tachycardia

In seven patients with documented ventricular tachycardia (VT) and prior myocardial infarction, late potentials (LP) were recorded at the end of or after the QRS complex from the body surface using high-gain amplification and the signal averaging technique (RC filter settings 100 to 300 Hz). In 6 to 7 patients VT could be initiated by programmed right ventricular stimulation; in one case, VT was inducible only from the left ventricle during surgery. Surgery was guided by epi- and endocardial mapping. In most cases besides resection of scar tissue, a partial or complete subendocardial encircling ventriculotomy was performed. Postoperatively, LPs were abolished in five cases, VT being no longer inducible. In the remaining two patients, LPs were still present. VT was still inducible in one of these two cases whereas in the other case, no programmed testing was done postoperatively. These data suggest that the abolition of LPs by surgery is closely related to the disappearance of the propensity to stimulus-induced VT. Thus, the averaging technique represents a new approach to the noninvasive control of the efficacy of surgery in patients with VT and prior myocardial infarction.

Endothelial tissue-type plasminogen activator release in coronary heart disease : Transient reduction in endothelial fibrinolytic reserve in patients with unstable angina pectoris or acute myocardial infarction

OBJECTIVESnWe sought to examine whether the disturbed fibrinolytic system in patients with an acute coronary syndrome is associated with a reduced endothelial fibrinolytic capacity.nnnBACKGROUNDnIntracoronary thrombus formation is a frequent finding in acute coronary syndromes. Systemic alterations of coagulation and fibrinolysis are known to occur, but possible disturbances of endothelial fibrinolytic function have not been investigated.nnnMETHODSnWe compared 42 patients with an acute coronary syndrome (acute myocardial infarction in 11 and unstable angina pectoris in 31) with 25 patients with stable angina. Venous blood was sampled serially for determination of markers of the fibrinolytic system and of hypercoagulability from admission to day 10. An occlusion test to determine the maximal endothelial tissue-type plasminogen activator (t-PA) release was also performed.nnnRESULTSnBoth on day 0 and day 10, patients with an acute coronary syndrome had a marked elevation of t-PA mass concentration (mean value +/- SEM 14.4 +/- 1.6 [day 0], 18.9 +/- 2.5 ng/ml [day 10]) and of plasminogen activator inhibitor (PAI) (9.4 +/- 2.2 [day 0], 11.3 +/- 2.6 AU/liter [day 10], p < 0.05 vs. patients with stable angina). There was also a hypercoagulative state with elevated thrombin activity and increased D-dimers (p < 0.05 vs. patients with stable angina). Maximal endothelial t-PA release was initially reduced (p < 0.05 vs. patients with stable angina) to 2.3 +/- 0.9 ng/ml, but levels recovered during follow-up to 4.4 +/- 1.4 ng/ml (vs. 5.7 +/- 1.5 ng/ml in patients with stable angina).nnnCONCLUSIONSnDespite the known prolonged systemic alteration of fibrinolysis in acute coronary syndromes, endothelial fibrinolytic capacity is reduced only during the acute phase and becomes normalized during follow-up, and thus is linked more to intravascular thrombus formation than to steady state levels of markers of the fibrinolytic system.

Comparison of the antiarrhythmic efficacy of disopyramide and mexiletine against stimulus-induced ventricular tachycardia.

Programmed ventricular stimulation was used to assess the effect of oral disopyramide (600 mg/day), mexiletine (600–1000 mg/day), and a combination of both drugs in a randomized cross-over study on 12 patients with documented ventricular tachycardia and/or fibrillation. In two cases, all three types of treatment were ineffective in that ventricular tachycardia could still be initiated under the same conditions. In four cases, disopyramide and mexiletine alone were ineffective or the change in inducibility was only slight. However, when both drugs were administered in combination, ventricular tachycardia was more difficult to induce or was no longer inducible. In two other cases, disopyramide was the more effective drug. In the remaining four patients, all three types of treatment were similarly effective. In patients whose ventricular tachycardia remained inducible its rate decreased from 188 ± 45 bpm (control) to 170 ± 40 bpm on disopyramide, 172 ± 31 bpm on mexiletine, and 146 ± 39 bpm on disopyramide plus mexiletine. Long-term therapy was based on the results of acute testing. Seven patients received both disopyramide and mexiletine and tolerated this therapy well during a follow-up of 42 ± 23 weeks. Two sudden deaths occurred, one possibly due to dose reduction and one in a patient in whom short bursts of ventricular tachycardia remained inducible during acute testing. We conclude that the combined administration of disopyramide and mexiletine is effective and safe in patients with ventricular tachycardia. It is tolerated without major side effects even during long-term therapy.

Effect of a single element subcutaneous array electrode added to a transvenous electrode configuration on the defibrillation field and the defibrillation threshold.

Even with the use of biphasic shocks, up to 5% of patients need an additional subcutaneous lead to obtain a defibrillation safety margin of at least 10 J. The number of patients requiring additional subcutaneous leads may even increase, because recent generation devices have a < 34 J maximum output in order to decrease their size. In 20 consecutive patients, a single element subcutaneous array lead was implanted in addition to a transvenous lead system consisting of a right ventricular (RV) and a vena cava superior lead using a single infraclavicular incision. The RV lead acted as the cathode; the subcutaneous lead and the lead in the subclavian vein acted as the anode. The biphasic defibrillation threshold was determined using a binary search protocol. Patients were randomized as to whether to start them with the transvenous lead configuration or the combination of the transvenous lead and the subcutaneous lead. In addition, a simplified assessment of the defibrillation field was performed by determining the interelectrode area for the transvenous lead only and the transvenous lead in combination with the subcutaneous lead from a biplane chest X ray. The intraoperative defibrillation threshold was reconfirmed after 1 week, after 3 months, and after 12 months. The mean defibrillation threshold with the additional subcutaneous lead was significantly (P = 0.0001) lower (5.7 ± 2.9 J) than for the transvenous lead system (9.5 ± 4.6 J). With the subcutaneous lead, the impedance of the high voltage circuit decreased from 48.9 ± 7.4 Ω to 39.2 ± 5.0 Ω. In the frontal plane, the interelectrode area increased by 11.3%± 5.5% (P < 0.0001) and in the lateral plane by 29.5%± 12.4% (P < 0.0001). The defibrillation threshold did not increase during follow‐up. Complications with the subcutaneous electrode were not observed during a follow‐up of 15.8 ± 2 months. The single finger array lead is useful in order to lower the defibrillation threshold and can be used in order to lower the defibrillation threshold.

Prognostic significance of repetitive ventricular response during programmed ventricular stimulation

Abstract To determine the incidence and prognostic significance of the repetitive ventricular response, a retrospective study was performed in 65 patients (49 male, 16 female, mean age ± standard deviation 55 ± 11 years) with coronary artery or myocardial disease and a variety of cardiac rhythm disorders. Programmed right ventricular stimulation was performed at a basic pacing rate of 120 beats/min using one (S 2 ) and two (S 2 -S 3 ) premature stimuli. The data were analyzed as to the presence or absence of a repetitive ventricular response and the patients outcome ([1] sudden death at 1 hour or less or documented ventricular fibrillation without myocardial infarction; [2] survival or death from noncardiac causes or nonsudden death). A repetitive ventricular response was observed in 23 (35.4 percent) of 65 patients after one and in 31 (48.4 percent) of 64 patients after two premature stimuli. It occurred in 9 of 9 patients with ventricular fibrillation and in 14 (82.4 percent) of 17 patients with ventricular tachycardia. The mean follow-up period was 76 ± 39 weeks. Sixteen patients were classified as dying suddenly; the remaining patients were considered surviving (or dying nonsuddenly). After one premature stimulus, a repetitive ventricular response was observed in 32.7 percent of patients surviving or with nonsudden death and in 43.8 percent of patients with sudden death or malignant ventricular arrhythmias. After two premature stimuli, the incidence of a repetitive ventricular response increased from 40.8 percent in patients surviving or with nonsudden death to 68.8 percent in patients with sudden death; 6 (12.2 percent) of 49 patients surviving or with non-sudden death and 9 (56.3 percent) of 16 patients with sudden death had more than three ventricular echo beats. All nonsurviving patients who demonstrated a repetitive ventricular response had intraventricular reentry. Depending on the rigidity of the criteria used (that is, the number of echo beats), the sensitivity of the test ranged between 37 and 88 percent and specificity ranged between 45 and 92 percent. The proportion of false positive results was high (33 to 66 percent); but the proportion of false negative results was low (8 to 18 percent). This retrospective study showed a correlation between sudden death and the incidence and number of repetitive ventricular responses (depending on the number of premature stimuli) and the type of reentrant beats (bundle branch reentry or intraventricular reentry).